and the mitochondrial epistatic genes CDK6 (implicated in neuronal cell cycle dysregulation, tau hyperphosphorylation, and neuroinflammation, with the YAP‐CDK6 axis noted as promising [47]) and IGF1R (where defects suggest resistance in AD neurons despite some benefits of IGF‐1 administration [48], supported by correlations of serum IGF‐1 levels with AD risk and resistance [49, 50]). This evidence concerns the gene IGF1 and Alzheimer disease.